Publications by authors named "Wenzhen He"

Article Synopsis
  • This study investigates the genetic risk factors for ischemic stroke (IS) subtypes by analyzing lipid metabolism and immune cell responses using Mendelian randomization (MR) methods.
  • Researchers found significant genetic associations between various lipids and risk factors for large artery stroke (LAS), small vessel stroke (SVS), and cardioembolic stroke (CS), identifying specific lipids as both risk and protective factors.
  • The study emphasizes the involvement of immune cells in mediating the relationship between lipids and IS, suggesting potential new therapeutic targets and enhancing understanding of the genetic factors driving IS.
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The accumulation and systemic propagation of senescent cells contributes to physiological aging and age-related pathology. However, which cell types are most susceptible to the aged milieu and could be responsible for the propagation of senescence has remained unclear. Here we found that physiologically aged bone marrow monocytes/macrophages (BMMs) propagate senescence to multiple tissues, through extracellular vesicles (EVs), and drive age-associated dysfunction in mice.

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Article Synopsis
  • Obesity leads to changes in the microRNA profile of extracellular vesicles released by bone marrow macrophages, which impact the differentiation of skeletal stem/progenitor cells (SSPCs) into either bone-building osteoblasts or fat-storing adipocytes, resulting in bone deterioration.
  • Macrophage-derived extracellular vesicles from obese mice cause significant bone loss when introduced to lean mice, while those from lean mice can improve bone health in obese mice.
  • Specific microRNAs, such as miR-140 and miR-378a, play opposing roles in regulating SSPC differentiation; targeting these microRNAs through an innovative delivery method restores bone health in obese mice, highlighting the role of bone marrow macrophages in obesity-related bone issues
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This practice guideline focuses on the cognitive assessment for mild cognitive impairment in the Guangdong-Hong Kong-Macao Greater Bay Area. To achieve the standardization and normalization of its clinical practice and generate individualized intervention, the National Core Cognitive Center of the Second Affiliated Hospital of Guangzhou Medical University, the Cognitive Disorders Branch of Chinese Geriatic Society, the Dementia Group of Neurology Branch of Guangdong Medical Association and specialists from Hong Kong and Macao developed guidelines based on China's actual conditions and efficiency, economic cost and accuracy. The article addresses the significance, background, and the process of the assessment and follow-up to realize the promotion and dissemination of cognitive assessment.

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Determining the manipulation unit of working memory is one of the fundamental questions in understanding how working memory functions. The prevalent object-based theory in cognitive research predicts that memory manipulation is performed on the level of objects. Here we show instead that the basic units of working memory manipulation are , a data structure describing what can be perceived in an instant.

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Mechanical forces are indispensable for bone healing, disruption of which is recognized as a contributing cause to nonunion or delayed union. However, the underlying mechanism of mechanical regulation of fracture healing is elusive. We used the lineage-tracing mouse model, conditional knockout depletion mouse model, hindlimb unloading model and single-cell RNA sequencing to analyze the crucial roles of mechanosensitive protein polycystin-1 (PC1, ) promotes periosteal stem/progenitor cells (PSPCs) osteochondral differentiation in fracture healing.

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The brain continually reorganizes its functional network to adapt to post-stroke functional impairments. Previous studies using static modularity analysis have presented global-level behavior patterns of this network reorganization. However, it is far from understood how the brain reconfigures its functional network dynamically following a stroke.

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Article Synopsis
  • SSPC senescence, which hinders bone healing as we age, is linked to factors secreted by macrophages in bone calluses, particularly grancalcin (GCA).
  • Injecting GCA into young mice triggered SSPC senescence and slowed down fracture healing, while removing the GCA gene from macrophages led to faster healing in older mice.
  • The study suggests that targeting GCA could be a potential treatment for improving fracture healing in older individuals suffering from nonunion or delayed fractures.
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Aims: It is estimated that 11.5% of patients with stroke (STR) were at risk of suffering poststroke epilepsy (PSE) within 5 years. Gut microbiota is shown to affect health in humans by producing metabolites.

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Immune system has been reported to play a key role in the development of ischaemic stroke (IS). Nevertheless, its exact immune-related mechanism has not yet been fully revealed. Gene expression data of IS and healthy control samples was downloaded from Gene Expression Omnibus database and differentially expressed genes (DEGs) was obtained.

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Purpose: The goal of our study is to uncover the pathogenesis of large-artery atherosclerotic ischemic stroke (LAAIS) and small-artery occlusion ischemic stroke (SAOIS) and analyze their difference using RNA sequencing.

Methods: RNA sequencing was used to filtrate differentially expressed mRNAs (DEmRNAs) and differentially expressed lncRNAs (DElncRNAs) in LAAIS and SAOIS. Specific DEmRNAs and DElncRNAs in LAAIS and SAOIS were further found.

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Article Synopsis
  • Type H vessels, a subtype of bone capillaries that express high levels of CD31 and endomucin, play a significant role in connecting bone growth (osteogenesis) and blood vessel formation (angiogenesis), but their numbers decrease with age.
  • The study identifies microRNA-188-3p (miR-188-3p) as a key player in this decline, with higher levels in aged skeletal endothelium that inhibit type H vessel formation by targeting integrin β3.
  • Mice lacking miR-188-3p showed improved preservation of type H vessels with age, while overexpressing it led to fewer type H vessels, lower bone mass, and slower bone healing, suggesting miR-
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Heterotopic ossification (HO) is defined as the occurrence of extraskeletal bone in soft tissue. Although this pathological osteogenesis process involves the participation of osteoblasts and osteoclasts during the formation of bone structures, it differs from normal physiological osteogenesis in many features. In this article, the primary characteristics of heterotopic ossification are reviewed from both clinical and basic research perspectives, with a special highlight on the influence of mechanics on heterotopic ossification, which serves an important role in the prophylaxis and treatment of HO.

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Among antiepileptic drugs (AEDs), sodium valproate alone or in the combination of topiramate (TPM) for treating refractory epilepsy was controversial. This meta-analysis aimed to systematically evaluate the clinical effects of these two regimens in this population. Relevant studies up to August 2021 were identified through systematic searches of CNKI, Wanfang, PubMed, and Embase databases.

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Skeletal aging is characterized by low bone turnover and marrow fat accumulation. However, the underlying mechanism for this imbalance is unclear. Here, we show that during aging in rats and mice proinflammatory and senescent subtypes of immune cells, including macrophages and neutrophils, accumulate in the bone marrow and secrete abundant grancalcin.

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Background: Ischemic stroke is a disease with high rate of death and disability worldwide. CircRNAs, as a novel type of non-coding RNAs, lacking 5' caps and 3' poly-A tails, has been associated with ischemic stroke. This study aimed to investigate key circRNAs related to ischemic stroke.

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Stroke (ST), endangering human health due to its high incidence and high mortality, is a global public health problem. There is increasing evidence that there is a link between the gut microbiota (GM) and neuropsychiatric diseases. We aimed to find the GM of ST, post-ST cognitive impairment (PSCI), and post-ST affective disorder (PSTD).

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The mammalian skeleton is a metabolically active organ that continuously undergoes bone remodeling, a process of tightly coupled bone resorption and formation throughout life. Recent studies have expanded our knowledge about the interactions between cells within bone marrow in bone remodeling. Macrophages resident in bone (BMMs) can regulate bone metabolism via secreting numbers of cytokines and exosomes.

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So far, the connections between obesity and skeleton have been extensively explored, but the results are inconsistent. Obesity is thought to affect bone health through a variety of mechanisms, including body weight, fat volume, bone formation/resorption, proinflammatory cytokines together with bone marrow microenvironment. In this review, we will mainly describe the effects of adipokines secreted by white adipose tissue on bone cells, as well as the interaction between brown adipose tissue, bone marrow adipose tissue, and bone metabolism.

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Osteoporosis and sarcopenia are two age-related diseases that affect the quality of life in the elderly. Initially, they were thought to be two independent diseases; however, recently, increasing basic and clinical data suggest that skeletal muscle and bone are both spatially and metabolically connected. The term "osteosarcopenia" is used to define a condition of synergy of low bone mineral density with muscle atrophy and hypofunction.

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Introduction: To evaluate effectiveness of human urinary kallindinogenase (HUK) in patients with acute ischemic stroke (AIS) according to Chinese ischemic stroke subclassification (CISS) and analyzed risk factors of clinical efficacy.

Methods: In this retrospective study, 134 patients received conventional therapy were enrolled to control group, and 132 patients received HUK treatment were enrolled to HUK group. National Institute of Health Stroke Scale (NIHSS) score was used to evaluate the clinical efficacy.

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Introduction: Ischemic stroke (IS) causes severe neurological impairments and physical disabilities and has a high economic burden. Our study aims to identify the key genes and upstream regulators in IS by integrated microarray analysis.

Methods: An integrated analysis of microarray studies of IS was performed to identify the differentially expressed genes (DEGs) in IS compared to normal control.

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Our previous study indicated that microRNA 145 (miR-145) and its predicated target, erythropoietin-producing hepatoma (EPH) receptor A4 (EPHA4), was closely associated with ischemic stroke. In this study, we aimed to further explore their function in a model of oxygen-glucose deprivation (OGD). The expression of miR-145 in the blood of 44 patients with ischemic stroke and 37 normal controls was detected by qRT-PCR.

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Objectives: To evaluate the effectiveness and safety of the combination of beraprost sodium (BPS) and aspirin in patients with acute ischemic stroke (AIS).

Methods: There were 384 patients with AIS enrolled in this single-center, retrospective study. The BPS group comprised patients who received combination therapy with BPS and aspirin, and the control group comprised those who received only aspirin.

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